The clinical picture of chronic hypertension—its symptoms, course, and complications—is quite clear but its causal factors and precipitating mechanisms cover a broad range. By causal factors we mean organic diseases; by precipitating mechanisms we mean personal habits and external influences that may foster the development of high blood pressure. It is essential that we distinguish between these two sets of circumstances. Whereas the causal agents are as a rule hereditary and appear spontaneously, the precipitating mechanisms can be controlled and eliminated.
Unfortunately we can identify only those causal factors with observable effects and which are linked to organic disease. The most common are inflammatory diseases of the kidneys, the various types of nephritis. But we know next to nothing about how and why they are linked to hypertension. We know a little more about the relationship between high blood pressure and various conditions that narrow the arteries of the kidneys (renal atrophy, hypoplasia, renal artery stenosis), thereby diminshing the blood supply to the kidneys and raising the blood pressure. It is possible that an increased production of a hormone-like substance, called renin by the defective kidneys provokes the onset of hypertension. The type of hypertension induced by kidney disease accounts for about 15% of all cases of chronic high blood pressure.
Among the rare causal factors are tumors—generally benign—of the adrenal glands, small organs about 2 inches in length lying above the kidneys. "They consist of two layers that produce hormones essential to the circulatory and metabolic functions of the body: the inner part (medulla) produces noradrenaline and adrenaline, which raise the blood pressure, and the outer part (cortex) secretes hydrocortisone and aldosterone which— indirectly—participate in the control of blood pressure. Tumors can stimulate the adrenals to excessive hormonal activity, which in turn can elevate the blood pressure to abnormally high levels. The incidence of this type of hypertension is low, about 1-2% of all cases. Another and highly infrequent type of hypertension is caused by a constriction of the aorta, the major artery leading from the heart (aortic coarctation).
These organically caused types of high blood pressure are referred to as "secondary hypertension," and they account for only about 16-18% of all known cases of high blood pressure. But in the overwhelming majority of all known cases no such causal factors exist. We refer to these as "primary" or "essential" hypertension.
Essential hypertension is a puzzling disease whose causes and nature are still largely unexplored. Put in its simplest form, it is a functional disorder of the nervous circuit controlling blood pressure. But despite intensive research we have not yet discovered the site of the defect—whether the pressure-sensitive receptors send out wrong information, whether the circulation center itself is defective and overstimulates the sympathico-adrenergic system, or whether the artery walls are unduly sensitized and react abnormally. All these questions remain unanswered.
A variety of factors, many unknown, apparently play a part in this puzzling malfunction of blood pressure regulation. We know that heredity plays an important role, as evidenced by the high incidence of essential hypertension running in families. Case histories show that the incidence of hypertension is greater among persons whose parents and grandparents suffered from high blood pressure or died of complications arising from it than among persons without a similar family history. Medical science knows next to nothing about the nature of this hereditary factor.
We know a great deal more about the environmental influences that can set off and accelerate both primary and secondary hypertension. They are: obesity, a high-sodium diet, and, possibly, prolonged psychological stress.
Excessive weight can enhance other risk factors and constitutes a serious health hazard. It is the crucial and at the same time most avoidable single known factor contributing to the development of high blood pressure. This was borne out emphatically by the Framingham study, which showed that persons whose weight was 20% above the norm run three times the risk of developing high blood pressure than those of normal weight. While the risk of hypertension increases with the amount of excess weight, weight loss can lower the pressure or even bring it down to normal.
Salt—the chemical sodium chloride—is an essential mineral required by the body. Whether salt is harmful to a person depends on his state of health and on how much salt he or she consumes. Ancient man, being a hunter and predator, lived on a low-salt diet, as do animals to this day. But as he learned to extract salt from the ocean and the earth he began to add it to his food. Salt became a seasoning in the preservation of meat and fish, and finally a major ingredient of our daily diet. The daily per capita salt consumption of Western man amounts to about 1/3-1/2 oz. (10-15g) whereas all we require is about 1/6 oz. (3-5g).
Animal experiments have shown that salt can in fact help raise our blood pressure. Among Eskimos, who eat very little salt, high blood pressure and stroke are very rare, while the Japanese, who are large salt consumers, have a high incidence of both. We also know that high salt intake can intensify an existing tendency toward hypertension while a low-salt diet can help keep it under control, as do certain drugs, the so-called diuretics, which stimulate the excretion of salt and are important in the treatment of the disease. The mechanism by which salt raises blood pressure is still unknown. All we know is that sodium plays the decisive role. Perhaps it is the content and distribution of sodium in the wall of the arteries that affects their sensitivity to sympathico-adrenergic stimulation.
Let us return briefly to the stress factor touched on earlier. According to a widely held belief tensions of all sorts can trigger high blood pressure. Job worries, social status, noise, aggression, agitation, anxiety, all these negative influences and emotions are thought to precipitate hypertension. But we have no definite proof that they do. What we do know is that they can raise the blood pressure temporarily and exacerbate existing hypertension. In some instances they can even turn "benign" hypertension into malignant hypertension. Even though conclusive evidence is still lacking we can safely assume that given a tendency toward hypertension—and only then—can frequent and prolonged stress facilitate and accelerate hypertension.